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Year 4 > Vascular > Flashcards

Vascular Flashcards

1
Q

define acute arterial ischaemia

A

acute occlusion of a peripheral artery, usually without Hx of claudication

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2
Q

Risk factors for developing acute arterial ischaemia

A

Conditions that predispose to embolism: arrhythmias, endocarditis, arterial aneurysms
atherosclerosis
previous vascular grafts
hypercoagulable states

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3
Q

symptoms of acute limb ischaemia

A 
pain
pallor
paraesthesia
paralysis
perishing cold
pulsless
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4
Q

investigations for acute ischiaemia

A 
ECG
troponin
FBC
PT/INR, PTT
echo
CTA
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5
Q

treatment of acute limb ischaemia

A 
heparin
embolectomy
thrombectomy
bypass graft
amputation
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6
Q

complications of reperfusion in acute ischaemia

A

compartment syndrome (with prolonged ischaemia)
arrhythmia and death
renal failure and multi-organ failure (toxic metabolites)

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7
Q

define chronic arterial occlusion/insufficiency

A

chronic ischaemia due to inadequate arterial supply to meet cellular metabolic demands

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8
Q

risk factors for chronic arterial insufficiency

A 
smoking
DM
age
HTN
hyperlipidaemia
obesity
sedentary
PMHx, FHx of CAD/CVD
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9
Q

cause of chronic arterial insufficiency

A

atherosclerosis

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10
Q

clinical features of chronic arterial insufficiency: claudication

A

pain with exertion that is relieved by a short rest and is reproducible

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11
Q

clinical features of chronic arterial insufficiency: critical limb ischaemia

A 
rest pain
night pain
tissue loss: ulercation, gangrene
pain over forefoot 
ABI < 0.4
absent pulses
signs of poor perfusion
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12
Q

DDx of claudication

A
  1. Vascular
    a. Atherosclerotic disease
    b. Vasculitis e.g. Buerger’s disease, Takayasu’s arteritis
    c. Diabetic neuropathy
    d. Popliteal entrapment syndrome
    1. Neurogenic
      a. Neurospinal disease e.g. spinal stenosis
      b. Complex regional pain syndrome
    2. MSK
      a. OA
      b. RA, connective tissue disease
      Remote trauma
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13
Q

list congenital hypercoagulable states

A 
Group I (reduced anticoagulants)
antithrombin
Protein C
Protein S
Group II (increased coagulants)
Factor V Leiden
Prothrombin
Factor VIII
Hyper-homocysteinemia
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14
Q

list acquired hypercoagulable state

A 
immobility
cancer
Pregnancy/systemic hormonal contraceptives/HRT
Antiphospholipid antibody syndrome
Inflammatory disorders (e.g. IBD)
Myeloproliferative disorders (e.g. ET)
Nephrotic syndrome (acquired deficit in Protein C and S)
DIC
HITT
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15
Q

type A vs B aortic dissection

A

A involves the ascending aorta but B does not

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16
Q

aetiology of aortic dissection

A 
most common HTN
others:
connective tissue disease - Marfans, Ehlers-Danlos
cystic medial necrosis
atherosclerosis
congenital conditions - coarctation, bicuspid aortic valves, PDA
syphillis
trauma
takayasus arteritis
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17
Q

investigaitons of aortic dissection

A

CTA
ECG and troponin
CXR
transoesphageal echo

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18
Q

what will a CXR show in aortic dissection

A

pleural cap
widened mediastinum
left pleural effusion

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19
Q

treatment of type A aortic dissection

A

resection of segment and replacement of graft

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20
Q

post operative complications of aortic dissection repair

A 
renal failure
intestinal ischaemia
stroke
paraplegia
persistent leg ischaemia
death
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21
Q

treatment of type B aortic dissection

A

IV antihypertensives
oral antihypertensives
b-blocker to decrease cardiac contractility

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22
Q

true vs false aneurysm

A

true - involves all vessel wal layers

23
Q

risk factors for aortic aneurysm

A 
smoking
HTN
PVD
CAD
CVD
age > 70
FHx
male
24
Q

aetiology of aortic aneurysm

A 
degeneraitve 
truamatic
mycotic - salmonella, staph
connective tissue disorder
vasculitis
infectious - syphilis, fungal
biscuspid aortic valves
25
Q

where are mycotic aortic aneurysm commonly found?

A

suprarenal

26
Q

what type of aortic aneurysms are associated with bicuspid aortic valves?

A

ascending thoracic aorta

27
Q

clinical features of aortic aneurysm

A 
asymptomatic
syncope
pain
hypotension
pulsatile, expansile mass
28
Q

what is the classic triad of a ruptured AAA

A

hypotension
back/abdo pain
expansile, pulsatile abdo mass

29
Q

investigations for an aortic aneurysm

A

FBC, U+E, creatinine, PTT, INR, group and save
abdo USS
CTA
peripheral arterial duplex

30
Q

conservative management of aortic aneurysm

A

cardiovascular risk factor reduction

31
Q

when would you surgically repair an aortic aneurysm

A

> 5.5.cm

32
Q

what does the risk of rupture of an aortic aneurysm depend on?

A 
size
FHx of rupture
rate of enlargement
symptoms
comorbities 
smokin
33
Q

what are the surgical options for repair of aortic aneurysm

A

open or EVAR

34
Q

complications of open aortic aneurysm repair

A

Early: renal failure, spinal cord injury (paraparesis or paraplegia), impotence, arterial thrombosis, anastomotic rupture or bleeding, peripheral emboli
Late: graft infection/thrombosis, aortoenteric fistula, anastomotic (psuedo) aneurysm

35
Q

complications of EVAR

A

Early: immediate conversion to open, groin haematoma, arterial thrombosis, iliac artery rupture, thromboemboli
Late: endoleak, graft kinking, migration. Thrombosis, rupture of aneurysm

36
Q

what is carotid stenosis?

A

narrowing of the internal carotid lumen due to atherosclerotic plaque formation, usually near bifurcation

37
Q

risk factors for carotid stenosis

A 
HTN
smoking
DM
CVD
CAD
dyslipidaemia
age
38
Q

clinical features of carotid stenosis

A

asymptomatic

hemispheric or ocular

39
Q

investigations for carotid stenosis

A

FBC, PT/INR, PTT
Fundoscopy – cholesterol emboli in retinal vessels (Hollenhorst plaques)
Auscultation over bifurcation for bruits
Carotid duplex – determines severity +/- cross sectional imaging with CT/M

40
Q

treatment of carotid stenosis

A

Risk factor modification
Dual antiplatelets
Surgical carotid endarectomy or endovascular angioplasty +/- stenting

41
Q

what are varicose veins?

A

distention of tortuous superficial veins resulting from incompetent valves in the deep, superficial or perforator systems

42
Q

causes of varicose veins

A 
age
oral contraceptive
prolonged standing
pregnancy 
obesity
Secondary: DVT, malignant pelvic tumours with venous compression, congenital anomalies, AV fistulae, trauma
43
Q

clinical features of varicose veins

A

Diffuse aching, fullness/tightness, nocturnal cramping
Aggravated by prolonged standing, premenstrual
Visible long, dilated, tortuous superficial veins (great or small saphenous + tributaries)
Ulceration, hyperpigmentation, and induration (ie lipodermatosclerosis)

44
Q

complications of varicose veins

A

Recurrent superficial thrombophlebitis/superficial vein thrombosis
Features of chronic venous insufficiency: ulceration, eczema, lipodermatosclerosis, stasis dermatitis and hyperpigmentation
Bleeding or haematoma secondary to trauma

45
Q

treatment of varicose veins

A

Cosmetic problem
Compression stockings
Indications for surgery: failure of conservative treatment, symptomatic varix (pain, bleeding, recurrent thrombophlebitis), tissue changes (hyperpigmentation, ulceration), cosmetic
Surgical: high ligation and stripping of the long saphenous vein and its tributaries, Ultrasound guided foam sclerotherapy, endovenous laser therapy

46
Q

what is chronic venous insufficiency?

A

Calf muscle pump dysfunction and valvular incompetence (reflux) due to phlebitis, varicositis, or DVT
Venous obstruction

47
Q

clinical features of chronic venous insufficiency

A

Pain, ankle and calf oedema – relieved by foot elevation
Pruritis, brownish hyperpigmentation (haemosiderin deposits)
Stasis dermatitis, SC fibrosis if chronic (lipodermatosclerosis)
Ulceration: shallow, above medial malleolus, weeping, painless, irregular outline
Signs of DVT/varicose veins/thrombophlebitis

48
Q

treatment of chronic venous insufficiency

A

Compression stockings
Ambulation
Periodic rest elevation
Avoid prolonged standing
Ulcers: multilayer compression bandage, antibiotics
Surgical ligation of perforators in region of ulcer
Endovenous: laser or radiofrequency ablation, or foam sclerotherapy

49
Q

what is lymphoedema

A

obstruction of lymphatic drainage resulting in oedema with high protein count

50
Q

primary causes of lymphoedema

A

Milroy’s syndrome: congenital hereditary lymphedema
Lymphoedema praecox (75% of cases): starts in adolescence
Lymphoedema tarda: starts >35 yr

51
Q

secondary causes of lymphoedema

A

Infection: filariasis (#1 cause worldwide)
Malignant infiltration: axillary, groin or intrapelvic
Radiation/surgery (axillary, groin lymph node removal)

52
Q

clinical features of lymphoedema

A

Classically non-pitting oedema

Impaired limb mobility, discomfort/pain, psychological distress

53
Q

treatment of lymphoedema

A

Avoid limb injury (can precipitate or worsen lymphedema)
Cellulitis: treat early to avoid further lymphatic damage
Skin hygiene
Daily skin care with moisturizers
Early medical assessment and treatment for infection (topical for fungal infection; systemic for bacterial infection)
External support
Intensive: compression bandages
Maintenance: compression garment
Exercise
Gentle daily exercise of affected limb, gradually increasing ROM
Must wear a compression sleeve/bandages when doing exercises
Massage: manual lymph drainage therapy

Year 4 (5 decks)

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